Therapeutic hyperventilation

The use of moderate hyperventilation is advocated for traumatic coma, but considerable controversy remains as to whether or not it is an effective or safe therapy. The rationale for hyperventilation is based on two premises. It reduces intracranial pressure and reverses cerebral lactic acidosis which, like intracranial hypertension, is correlated with poor outcome after brain injury.

The fall in intracranial pressure induced by hyperventilation occurs secondary to constriction of cerebral vessels and a consequent reduction in cerebral blood flow and volume. Cerebral blood flow decreases by about 15 per cent for each 0.5-kPa reduction in PaCO2. The reactivity of cerebral vessels to CO2 appears to be maintained in many patients following head injury, and this argues for the effectiveness of hyperventilation as a therapy for intracranial hypertension. As might be expected, the response to hyperventilation is greatest in those with cerebral hyperemia or 'luxury perfusion'. Since these are the patients who are most likely to develop intracranial hypertension, their relatively greater responsiveness may be of therapeutic significance. However, following closed head injury some patients develop a phase of low cerebral blood flow which may persist for 12 to 24 h. Such patients may be at risk of cerebral ischemia following a further reduction in cerebral blood flow by hyperventilation.

Hyperventilation also reverses the cerebral metabolic acidosis commonly present after head injury. As CO 2 freely passes the blood-brain barrier, the respiratory alkalosis produced by hyperventilation causes cerebral CO 2 to be depleted. The restoration of cerebral autoregulation in patients with global hyperemia is likely to be related to this reversal of cerebral acidosis.

Changes in cerebral blood flow and intracranial pressure may become refractory to hyperventilation because of a normalization of the intracellular and extracellular pH of the central nervous system by the bicarbonate buffering mechanism. In some cases accumulation of lactic acid within the brain may also play a part; this may be due to excessive hyperventilation which can lead to the development of cerebral ischemia and cerebral lactic acidosis. This may explain why patients with cerebral hyperemia are least refractory to prolonged hyperventilation. Maintenance of the reactivity of cerebral vessels to CO 2 does not ensure continued control of intracranial pressure, as progressive brain edema might outweigh the effects of intracranial pressure from therapeutic decreases in cerebral blood volume. It has also been shown that unacceptable rises in intracranial pressure can occur when hyperventilation is withdrawn after many days.

Other beneficial effects of hyperventilation might include a reduction in energy requirement because of the reduced work of breathing and a reduction in cerebrospinal fluid formation, although these are unlikely to be of clinical significance.

An inverse steal (Robin Hood phenomenon) has been reported in severe head injury and brain tumors following hyperventilation. Blood flow to uninjured brain is reduced by hyperventilation, while the cerebral vessels in the injured area do not constrict and blood flow is preferentially diverted to that area.

Hyperventilation can also have deleterious effects. By reducing cerebral blood flow, hyperventilation may change borderline cerebral ischemia into full-blown ischemia. For example, active hyperventilation of awake unsedated subjects to a PaCO2 of 2.7 kPa induces electroencephalographic changes compatible with cerebral hypoxia. In some comatose patients treated with prolonged hyperventilation, an improvement in conscious level has been seen when the PaCO2 was allowed to return to normal values.

One of the supposed benefits of hyperventilation is the induction of an inverse steal phenomenon as described above. However, recent evidence suggests that, under certain circumstances, preferential blood flow to the injured area may result in progressive edema in this area and a consequent reduction in local oxygen supply.

Hyperventilation causes a leftward shift of the oxygen-hemoglobin dissociation curve and inhibition of oxygen delivery to the tissues. This will reduce oxygen delivery to the brain and may also reduce cardiac output if myocardial oxygen delivery is impaired. Artificial ventilation increases mean intrathoracic pressure, and this may further decrease cardiac output and adversely affect cerebral blood flow. Large increases in intrathoracic pressure can indirectly increase intracranial pressure because of the rise in central venous pressure.

If adaptation to prolonged hyperventilation occurs, rebound intracranial hypertension may result when hyperventilation is discontinued. As the central nervous system pH is decreased via the buffering mechanism during adaptation, a relative central nervous system acidosis and concomitant rise in cerebral blood flow can occur as the PaCO2 is allowed to rise. This will persist until the buffering system has had time to recorrect the pH.

No controlled clinical studies have shown an improvement in outcome when prolonged hyperventilation is used as a therapy for intracranial hypertension. There has been a trend away from the use of empirical hyperventilation and towards limiting the drop in PaCO2 to moderate levels in those in whom it is indicated. A PaCO2 of 4.0 to 4.5 kPa is now accepted as being the endpoint for therapeutic hyperventilation in many units. Monitoring must also be used to titrate hypocapnea, so that reductions in intracranial pressure are achieved while cerebral oligemia is avoided. Monitoring of jugular venous saturation ( SjO2) has been used to assess the relative adequacy of cerebral oxygen supply.

Although the reduction in cerebral blood volume may be small compared with total brain volume, hypocapnia can be lifesaving in patients with an expanding cerebral lesion.

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